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EGFR activates AKT1. 31 / 74
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"In turn, EGFR sequentially activates phosphatidylinositol-3 kinase (Pi3k) and its downstream effectors protein kinase B (PKB/Akt), p38 Mapk, Erk1/2 and, protein kinase Cζ (PKCζ) [22, 23] ."

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"Using an external scoring function (TIGER software) for target prediction proved useful in this study, complementing the twin-CLM approach.To confirm the biological activities of the most potent compounds 18 (K  = 52 nM) and 22 (K  = 13 nM) in cells, we tested compound effects on epidermal growth factor receptor (EGFR)-induced activation of AKT/protein kinase B (PKB), a well-established effector downstream of EGFR-PI3K signaling in cancer ."

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"Upon activation, EGFR undergoes dimerization and endocytosis, during which EGFR upregulates AKT1, STAT3 and RAS signaling pathways to promote DNA synthesis and cell proliferation [36] ."

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"The results showed that TS inhibited the growth of gastric cancer by down-regulating the expression of EGFR and AKT1 in cancer cells and inhibiting the EGFR/AKT1 signaling pathway [128]."

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"Inhibition of EGFR activation by novel small molecules or by short hairpin RNA knockdown in Ang II treated SV40 mesangial cells in vitro suppresses protein kinase B and extracellular signal related kinase signaling pathways and transforming growth factor-beta and Sma- and Mad related protein activation, and abolishes the accumulation of fibrotic markers such as connective tissue growth factor, collagen IV."

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"The activation of EGFR in trametinib‐treated cells, in turn, stimulated hyperactivation of the phosphatidylinositol‐4,5‐bisphosphate 3‐kinase/protein kinase B (PI3K/AKT) pathway as a compensatory survival mechanism."

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"Both EGFR and FYN also activate AKT1 toward tau, reinforcing the key role of AKT1."

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"Here we show that cholesterol depletion by beta-cyclodextrin disrupts caveolae structure and concomitantly inhibits tyrosine phosphorylation of the EGF-R and subsequent activation of protein kinase B (PKB)/Akt induced by angiotensin II."

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"The study provided evidence that Akti-1/2 ultimately induces the expression and activation of receptor tyrosine kinases EGFR, HER3, and HER4, which in turn reactivate Akt1 [54]."

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"Previous studies indicated that EGFRvIII expressing cells constitutively activate phosphatidylinositol 3-Kinase (PI3-K) and Akt1, and that Akt1 can inhibit HRR by inducing cytoplasmic retention of Rad51."

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"Collectively, these results suggested the activation of EGFR mediates β-catenin nuclear accumulation in Akt1-impaired breast cancer cells."

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"Because AKT1 can be activated by the EGFR signaling to enhance cancer cell survival, it is possible that the AKT1 activity may be further exaggerated due to the augment of both EGFR and AKT1 gene copy numbers and result in a worse 5-year OS than patients with an increase in EGFR gene copy numbers alone."

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"EGFR activation is mediated by mitogen-activated protein kinase (MAPK), phosphoinositide 3-kinase (PI3K), and protein kinase B (AKT) pathways."

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"Activation of EGFR triggers three main signaling pathways : the ERK pathway, the PI3K and protein kinase B (Akt) pathway, and the Jakus kinase (JAK)/signal transducer and activator of transcription protein (STAT) pathway."

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"We observed that inhibition of EGFR kinase activity with AG1478 significantly attenuated H2O2 induced p38 (SAPK) and ERK1/2 activation, but did not inhibit Akt1 activation."

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"On the other hand, up-regulation of EGFR has been observed to activate AKT1 XREF_BIBR."

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"Our study showed that the chemical components of Sedanolide, Ligustilide, α-Terpineol, 4-Terpineol, Senkyunolide H, and Senkyunolide I in JBOL might act on the signaling pathway such as AGE-RAGE, EGFR, PI3K-Akt, and HIF-1 by modulating AKT1, STAT3, EGFR, IL-1β, and SCR, thus exerting an anti-IPF effect."

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"Moreover, while ligand-activated EGFR stimulates both the RAS-RAF-MAPK and PI3K-Akt-1 pathways ( xref ), EGFRvIII preferentially activates PI3K-Akt-1 ( xref , xref )."

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"In this clustering module, other nodal proteins are directly or indirectly involved in Akt1 activation, such as the extracellular-associated factors, VEGFA and EGFR, which bind to dimerize the protein [47]."

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"Sevelda et al. showed that Egfr increased starvation resistance through interactions with Akt1 [64]."

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"In future studies, it will be important to elucidate the precise mechanism by which PI3K-Akt-1 activation by EGFRvIII might promote DNA-PKcs hyperactivation in GBM tumor cells."

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"Both EGFR and FYN also activate AKT1 toward tau, reinforcing the key role of AKT1."

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"For example, up-regulation of lncRNA LINC00152 promoted the development of non-small cell lung cancer (NSCLC) through activating EGFR, which promoted tumor cell proliferation by increasing the activity of the PI3K/Akt (AKT serine/threonine kinase 1) pathway [33]."

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"Blockage of radiation induced DNA-PKcs activation by EGFR, PI3-K or AKT inhibition as well as through knockdown of AKT1 by siRNA indicates the requirement of the EGFR-PI3-K and AKT pathway for the reg[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"If LRP‐1 is the bLF receptor, its stimulation by bLF would lead to the activation of Scr kinases activating tyrosine kinase (Trk) receptors, such as EGFR, that in turn would increase pERK and pAKT (Mao et al., 2017; Shi et al., 2009)."

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"Unfortunately, in mouse models, the resulting mitogen-activated protein kinase (MAPK) inhibition after KRAS inhibition (or direct blockade of downstream MEK) may further lead to the activation of protein kinase B alpha (Akt), EGFR, human epidermal growth factor receptor 2 (HER2), platelet-derived growth factor receptor α (PDGFRα), and AXL, resulting in the ineffectiveness of such drugs[15]."

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"In 20% of the cases, EGFR presents a mutation (EGFRvIII) that constitutively activates the PI3K/protein kinase B (Akt)/mTOR pathway, making EGFR inhibitors an alternative therapy to control or treat the GB [7,8]."

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"In summary, these studies indicate that EGF signaling through EGFR activates PKBalpha and AKT as a principal target, and blocking this pathway with the EGFR specific tyrosine kinase inhibitor, Iressa, results in programmed cell death."

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"The alleviating effect of baicalin on fatty liver may be related to the up-regulation of solute vector family member 4 (SLC2A4), Down-regulated AKT serine/threonine kinase 1 (AKT1), Peroxisome proliferator-activated receptor gamma (PPARG), Epidermal growth factor receptor (EGFR), tumor necrosis factor (TNF), Interleukin 6 (IL-6) were associated."

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"EGFR with activating mutations was seen to activate the protein kinase B (Akt) pathway rather than the extracellular signal-regulated kinases (ERK) pathway, and NSCLC tumors highly positive for phosph[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"In turn, EGFR sequentially activates PI3K and its downstream effectors protein kinase B (PKB/AKT), P38 MAPK, Erk1/2, and PKC zeta [5,6] ."